[Bile flow and bile acid excretion in rats fed a fat-rich diet in relation to the fatty-acid pattern of the diet and to additionally applied cholic acid].
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Animals↗
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Plasma clearance of oral and intravenous cholic acid in subjects with and without chronic liver disease.
The apparent plasms clearances of tracer amounts of radiolabelled cholic acid given orally or intravenously were compared in 14 control subjects and 20 patients with chronic liver disease. The clearance after oral administration was the more sensitive in detecting chronic liver disease and correlated better with the fasting levels of endogenous serum bile acid. This agrees with the predicted effects on clearance of hepatocellular damage and portal-systemic shunting of blood after the two routes of administration. The estimated hepatic extraction ratio, calculated from the ratio of the oral and intravenous clearances, was 0.77+/-0.02 (mean+/-SEM) in control subjects, 0.64+/-0.03 in patients with anicteric chronic liver disease, and 0.46+/-0.05 in those with icteric chronic liver disease.
Administration, Oral↗
Immunoassay of serum conjugates of cholic acid in cystic fibrosis.
Pre- and post-prandial serum conjugates of cholic acid (SCCA) were measured by radioimmunoassay (RIA) in 83 patients with cystic fibrosis (CF), 14 of whom did not have steatorrhoea, and in 25 controls. Of the CF patients with steatorrhoea, 38% had fasting SCCA levels greater than 3 standard deviations above mean fasting control values, whereas no CF patient without steatorrhoea had elevated fasting SCCA levels. Steatorrhoeic patients with palpable livers had higher pre- and post-prandial SCCA levels. Post-prandial SCCA levels failed to discriminate between control and CF groups however. Other serum tests of liver function, including the aspartate amino transferase, alkaline phosphatase, albumin, gamma globulin, and albumin : globulin ratio, failed to correlate with the SCCA. Changes in serum protein constituents correlated strongly with pulmonary dysfunction. The results suggest that elevation of fasting SCCA levels in CF patients is a more sensitive indicator of liver dysfunction than other tests and is a better discriminator than post-prandial SCCA levels between normal and abnormal liver function. The test is recommended for early detection of liver dysfunction in CF patients.
Adolescent↗
Different effects on the expression of CYP7 and CYP27 in rabbit liver by cholic acid and cholestyramine.
It was recently reported that both cholesterol 7 alpha-hydroxylase CYP7 and sterol 27-hydroxylase CYP27 are subject to negative feedback control by bile acids in isolated rat hepatocytes and rat liver (Twisk et al., (1995) Biochem. J. 305, 505-511; Vlahcevic et al. XIII International Bile Acid Meeting, September 30-October 2, 1994, Abstract 17). In the present work a series of experiments was performed to study whether there is a coordinate regulation of CYP7 and CYP27 also in rabbit liver. Treatments of rabbits with cholic acid or cholestyramine resulted in marked suppression and induction, respectively, of CYP7 mRNA. In contrast, there were no significant effects on the CYP27 mRNA expression, amount of CYP27 protein or mitochondrial 27-hydroxylase activity. Thus, there is an apparent difference between rat and rabbit with respect to regulation of CYP27 by bile acids. It is concluded that, in rabbit, there is little or no coordinate regulation of CYP7 and CYP27 at a transcriptional level, and that CYP27 is not subject to a negative feedback control by bile acids neither at a transcriptional nor at a posttranscriptional level.
Animals↗
Ability of aberrant crypt foci characteristics to predict colonic tumor incidence in rats fed cholic acid.
Aberrant crypt foci (ACF) are putative preneoplastic lesions of colon cancer which are being utilized currently as a biological end point to evaluate the induction and modulation of colon carcinogenesis. In several previous short-term studies, the unexpected reduction of ACF by the reported colonic tumor promoter cholic acid (CHA) emphasized the need for a systematic evaluation of the growth of ACF in response to a tumor promoter. The present study was conducted to determine if any characteristic(s) of ACF at various early stages of carcinogenesis would predict resulting tumor incidence in rats fed CHA. Male Sprague-Dawley rats received two injections of azoxymethane (20 mg/kg) and were fed either the AIN-76 diet or AIN-76 plus 0.2% CHA. The number, crypt multiplicity (number of crypts/focus), and size (area) of ACF were measured after 2, 8, 14, and 18 weeks in 5 rats/group. The number of ACF was lower (P < 0.033) in animals fed CHA at all time points. Average crypt multiplicity of ACF was greater (P = 0.045) from CHA-fed animals after 8 weeks compared to animals fed the AIN-76 diet. The average size of ACF was smaller in CHA-fed animals after 2 weeks and then tended to be larger than the sizes of the ACF from animals fed the AIN-76 diet. All remaining animals were killed after 18 weeks. Tumor incidence was higher (P < 0.001) in the CHA-fed group (63.2%) compared to the control diet group (29.4%). CHA-fed rats also had a higher number of tumors/tumor-bearing rat compared to control diet rats (1.96 versus 1.13). The main finding of this study is that the number of ACF at early time points did not predict tumor incidence. Crypt multiplicity was a consistent predictor of tumor outcome and should be measured in future studies using ACF as a biological end point. The CHA diet appears to provide a unique tumor-modulating environment that selectively enhances the growth of a smaller number of ACF leading to an increased number of tumors compared to a control diet. The mechanism(s) by which CHA mediates this effect warrants further investigation.
Animals↗
Prevention of TCDD toxicity in laboratory rodents by addition of charcoal or cholic acids to chow.
The mortalities of mice, rats and guinea-pigs given a single lethal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were substantially reduced by feeding them with chows containing 2.5 or 5% activated charcoal, which presumably enhances elimination of the toxic agent from the organism. Chows with 0.25 or 0.5% cholic acid and dehydrocholic acid added had a similar protective action on mice intoxicated with TCDD. Since no treatment is currently available for this type of poisoning, charcoal-whose safe clinical use is well established-is worth considering in view of its potential benefit to humans acutely exposed to TCDD.
Animal Feed↗
Carbon tetrachloride-induced hepatotoxicity enhances the development of pulmonary foam cells in rats fed a cholesterol-cholic acid diet.
The effect of CCl4-hepatotoxicity on the development of pulmonary foam cells (PFCs) was studied using 4 groups of rats. Rats in the control group were fed a standard diet; rats in the second group were fed a hyper beta-lipoproteinemic (HB) diet consisting of the standard diet, 4% cholesterol, and 1% cholic acid; rats in the third group were fed the standard diet and administered with CCl4 (1.0 ml/kg, i.p., fortnightly) (CT); and rats in the fourth group were fed the HB diet and administered with CCl4 (HT). At feeding week 10, rats in the HB and HT groups developed hyper beta-lipoproteinemia. The ratios of foamy, lipid-ingested monocytes (FMs) to blood monocytes (BMs) and the histologic scores of PFC development were significantly greater in the HB and HT groups than in the control and CT groups, respectively. The ratio of PFCs to alveolar macrophages from bronchopulmonary lavage fluid was significantly higher in the HT group than in the CT group. At feeding week 20, rats in the CT and HT groups suffered hepatic injury and hypo beta-lipoproteinemia. Despite hypo beta-lipoproteinemia, the FM and PFC development, the ratio of BMs in differential leukocyte counts, and latex-phagocytotic activity of BMs were enhanced in the HT group. Furthermore, markedly enlarged FMs, described here as giant-FMs, that contained numerous lipid droplets in their abundant cytoplasm appeared in the peripheral blood from rats in the HT group. Histologically, embolism caused by giant-FMs in the pulmonary blood vessels and intraalveolar accumulation of PFCs were detected with a high incidence in the HT group. The present study suggests that CCl4-hepatotoxicity may affect lipoprotein synthesis in the liver of hyper beta-lipoproteinemic rats and defective or modified lipoproteins can be phagocytosed actively by BMs, and then BMs transform into FMs or giant-FMs, resulting in the PFC development and pulmonary embolism by giant-FMs.
Animals↗
Cholic acid binding by glutathione S-transferases from rat liver cytosol.
Cholic acid-binding activity in cytosol from rat livers appears to be mainly associated with enzymes having glutathione S-transferase activity; at least four of the enzymes in this group can bind the bile acid. Examination of the subunit compositions of different glutathione S-transferases indicated that cholic acid binding and the ability to conjugate reduced glutathione with 1,2-dichloro-4-nitrobenzene may be ascribed to different subunits.
Animals↗
On the conjugation and formation of bile acids in the human liver. II. On the conjugation of cholic acid (-2414C) in human liver homogenates; bile acids and steroids 62.
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Bile Acids and Salts↗
On the conjugation and formation of bile acids in the human liver. III. On the conjugation of cholic acid (-2414C) in microhomogenates of the human liver; bile acids and steroids 63.
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Bile Acids and Salts↗
[Utilization of bile acids and cholesterol by microorganisms consuming cholic acid].
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Actinomyces↗
The evolution of morphologic changes in the gallbladder before stone formation in mice fed a cholesterol-cholic acid diet.
Mice were fed a lithogenic diet containing 1% cholesterol and 0.5% cholic acid, and the sequence of morphologic changes in the gallbladder was followed. Histologic changes were studied with light microscopy and cell proliferation with autoradiography. Mucus glycoprotein production was studied with a spectrum of glycoprotein histochemical stains and electron-microscopic morphometry of membrane-bound mucus secretory granules. There was a rapid and early increase in cell proliferation of the epithelial cells and an increase in mucus production, which took place long before any observable cholesterol crystal precipitation. The gallbladder epithelial cells showed early focal pseudostratification and large numbers of degenerative cells. These changes culminated in glandular metaplasia and the formation of Rokitansky-Aschoff sinuses later in the gallstone induction phase. These observations clearly indicated that gallbladder epithelial injury had taken place before gallstone formation. The authors hypothesize that the consequences of these cellular changes play a contributory role in causing gallstone formation.
Animals↗
Regulation of sterol 12alpha-hydroxylase and cholic acid biosynthesis in the rat.
BACKGROUND & AIMS: Sterol 12alpha-hydroxylase (CYP8b1) is required for the biosynthesis of cholic acid (CA) and hence helps determine the ratio of CA to chenodeoxycholic acid (CDCA) in bile. This study examined the in vivo regulation of CYP8b1 in the rat by bile acids, cholesterol, and thyroxine. METHODS: The specific activities (SAs), messenger RNA (mRNA) levels, and transcriptional activities of CYP8b1 were determined in intact rats and rats with biliary diversion. RESULTS: CA, CDCA, and deoxycholic acid (DCA), fed as a supplement to the diet, down-regulated CYP8b1 SAs by 99% +/- 0%, 72% +/- 10%, and 98% +/- 1%, respectively. Under these same conditions, mRNA levels decreased by 93% +/- 7%, 60% +/- 11%, and 93% +/- 4%, respectively. Intraduodenal infusion of taurocholate (36 micromol/h. 100 g rat(-1)) decreased SAs and mRNA levels by 63% +/- 8% and 74% +/- 8%, respectively. Ursodeoxycholic acid (UDC) and hyocholic acid (HC) feeding increased CYP8b1 SAs by 119% +/- 21% and 65% +/- 18%, respectively. CA feeding decreased CYP8b1 transcriptional activity by 72%. Complete biliary diversion increased CYP8b1 SAs and mRNA levels by 150% +/- 30% and 287% +/- 51%, respectively. Cholesterol feeding decreased CYP8b1 mRNA by 39% +/- 8%. In intact rats, a single injection of thyroid hormone eliminated CYP8b1 activity. CONCLUSIONS: CYP8b1 is transcriptionally down-regulated by hydrophobic but not hydrophilic bile acids. Cholesterol feeding and a single thyroid hormone injection repressed CYP8b1 in the face of induction of cholesterol 7alpha-hydroxylase (CYP7a1 by the new nomenclature) SAs. These results suggest that cholesterol, thyroid hormone, and hydrophobic bile acids are important regulators of CYP8b1 and consequently of the bile acid pool composition.
Animals↗
Cholic acid as key regulator of cholesterol synthesis, intestinal absorption and hepatic storage in mice.
To study the effects of cholic acid (CA) feeding on hepatic cholesterol metabolism, male sterol 12alpha-hydroxylase (CYP8B1) knockout (-/-) mice and wildtype controls (+/+) were fed either a control diet or the same diet supplemented with CA (0.1% or 0.5% w/w) or cholesterol (1% w/w). During feeding of the control diet, cholesterol synthesis was increased in CYP8B1-/- compared to +/+ mice. Both cholesterol and CA feeding down regulated mRNA expression of cholesterogenic genes and hepatic de novo cholesterol synthesis as also reflected by a concomitant decrease in the nuclear factor SREBP-2 precursor protein and increased hepatic free cholesterol levels. Mice with an intact CYP8B1 gene (CYP8B1+/+ and C57Bl/6 mice) accumulated higher concentrations of cholesteryl esters (24- and 25-fold, respectively) in their livers compared to CYP8B1-/- mice (8-fold). Feeding of CA increased intestinal cholesterol absorption in CYP8B1+/+ mice by 23% and in CYP8B1-/- mice by 50%. While plasma cholesterol did not differ between CYP8B1+/+ and -/- mice under control conditions and cholesterol feeding a decrease was seen in CYP8B1-/- but not CYP8B1+/+ mice fed CA. This study indicates that CA is an important determinant for intestinal cholesterol absorption and that the levels of the transcription factor SREBP-2 in the liver are dependent upon the combined effect of CA on intestinal cholesterol absorption and CYP7A1. The possibility is discussed that inhibition of CYP8B1 and thus CA synthesis may be beneficial for the treatment of hyperlipidemic disorders.
Animals↗
[Quantitative determination of cholic acid in Calulus Bovis].
OBJECTIVE: To establish a method to determine the Content of cholic acid in Calulus Bovis. METHOD: The content was determined by TLCS. RESULT: Recovery rate was 96.54%, RSD was 1.68%. CONCLUSION: Accurate and reproducible, this method can be used for the quality control of Calulus Bovis.
Animals↗
Bile acids. LII. The synthesis of 24-nor-5alpha-cholic acid and its 3beta-isomer.
To aid in the identification of trihydroxy acidic metabolite(s) derived from beta-sitosterol, 3alpha,7alpha,12alpha-trihydroxy-24-nor-5beta-cholan-23-oic acid was prepared and its methyl ester was treated with Raney nickel in boiling p-cymene to provide methyl 3-oxo-7alpha,12alpha-dihydroxy-24-nor-5alpha-cholanate, 3-oxo-7alpha,12alpha-dihydroxy-24-nor-5beta-cholante and 3-oxo-7alpha,12alpha-dihydroxy-24-norchol-4-enoate. The latter compound was synthesized from the 3-oxo-5beta-derivative with SeO2 to provide a product with identical properties. Catalytic reduction of either saturated 3-oxo-derivative provided the appropriate 3,7,12-triols isomeric at C-3. Results from gas liquid and partition chromatography, mass spectrometry, and otherr physical properties of the acids, their methyl esters and other derivatives are compatible with the assigned structures.
Chemical Phenomena↗
Synthesis of 3 alpha,7 alpha,12 alpha,25-tetrahydroxy-5 beta-cholestan-24-one, an intermediate in the 25-hydroxylation pathway of cholic acid biosynthesis from cholesterol.
This paper describes the chemical synthesis of 3 alpha,7 alpha,12 alpha,25-tetrahydroxy-5 beta-cholestan-24-one via selective oxidation of 5 beta-cholestane-3 alpha,7 alpha,12 alpha, 24 xi,25-pentol with silver carbonate on celite. The structure of this 24-keto bile alcohol was confirmed by gas-liquid chromatography and mass spectrometry. Synthesis of this compound via pyridinium chlorochromate oxidation of the triacetoxy derivative of 5 beta-cholestane-3 alpha,7 alpha,12 alpha,24 xi,25-pentol followed by saponification further established its structure. 3 alpha,7 alpha,12 alpha,25-Tetrahydroxy-5 beta-cholestan-24-one was required for the in vivo and in vitro studies of side-chain oxidation and cleavage in the 25-hydroxylation pathway of cholic acid biosynthesis.
Cholestanols↗
7 alpha-Dehydroxylation of cholic acid by cell extracts of Eubacterium species V.P.I. 12708.
NADH:flavin oxidoreductase and 7 alpha-dehydroxylase were induced 5- and 90-fold, respectively, by cholic acid in cultures of Eubacterium species V.P.I. 12708. Assays of 7 alpha-dehydroxylase activity in the presence of various cofactors revealed that optimal activity was obtained in the presence of NAD+ plus FADH2. The pH optima of 7 alpha-dehydroxylase activity in whole cells and cell extracts were 7.0. The similar induction pattern of these two enzymes and the apparent cofactor requirements for 7 alpha-dehydroxylation suggest a relationship between 7 alpha-dehydroxylase and NADH:flavin oxidoreductase.
Bile Acids and Salts↗